Skewed differentiation of bone marrow CD34+ cells of tumor bearers from dendritic toward monocytic cells, and the redirection of differentiation toward dendritic cells by 1α,25-dihydroxyvitamin D3

Young, Matthew R.; Wright, M. A.; Vellody, K.; Lathers, Deanne

doi:10.1016/s0192-0561(99)00044-2

Cited by 22 publications

(9 citation statements)

References 30 publications

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“…Populations of CD11b + /Gr1 + myeloid cells are significantly expanded in the bone marrow and spleens of cancer-bearing mice relative to cancer-free counterparts 46,47 , and their numbers are also increased in the circulation of cancer patients compared with cancer-free subjects 48,49 . Experiments using mouse models of mammary carcinoma expanded on these observations by demonstrating that when CD11b + /Gr1 + myeloid cells were isolated from the spleens of mice bearing mammary tumours and were mixed with tumour cells before implantation, tumour growth and metastasis were enhanced 50 .…”

Section: Tumour-driven Systemic Processes That Affect Primary Tumour mentioning

confidence: 97%

The tumour-induced systemic environment as a critical regulator of cancer progression and metastasis

2014

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Recent pre-clinical and clinical research has provided evidence that cancer progression is driven not only by a tumour’s underlying genetic alterations and paracrine interactions within the tumour microenvironment, but also by complex systemic processes. We review these emerging paradigms of cancer pathophysiology and discuss how a clearer understanding of systemic regulation of cancer progression could guide development of new therapeutic modalities and efforts to prevent disease relapse following initial diagnosis and treatment.

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Section: Tumour-driven Systemic Processes That Affect Primary Tumour mentioning

confidence: 97%

The tumour-induced systemic environment as a critical regulator of cancer progression and metastasis

2014

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“…Similarly, curcumin induced differentiation of MDSCs into M1-type macrophages through interaction with JAK2/STAT3 80 . Although an involvement of STAT signaling has not been reported, 1α,25-hydroxyvitamin D3 induced differentiation of CD34 + immature cells into mature DCs in both tumor-bearing mice and HNSCC patients 81,82 . Treatment of HNSCC patients with vitamin D3 before tumor resection resulted in higher levels of intratumoral CD8 + T cells and prolonged recurrence-free survival, which could be due to its effect on MDSCs 83 .…”

Section: Myeloid-derived Suppressor Cellsmentioning

confidence: 98%

Improving cancer immunotherapy by targeting the STATe of MDSCs

et al. 2016

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Cancer immunotherapy is a promising therapeutic avenue; however, in practice its efficacy is hampered by an immunosuppressive tumor microenvironment that consists of suppressive cell types like myeloid-derived suppressor cells (MDSCs). Eradication or reprogramming of MDSCs could therefore enhance clinical responses to immunotherapy. Here, we review clinically available drugs that target MDSCs, often through inhibition of STAT signaling, which is essential for MDSC accumulation and suppressive functions. Interestingly, several drugs used for non-cancerous indications and natural compounds similarly inhibit MDSCs by STAT inhibition, but have fewer side effects than anticancer drugs. Therefore, they show great potential for combination strategies with immunotherapy.

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“…CD34 + cells are a part of a spectrum of immature myeloid-lineage cells, the levels of which become prominent in HNSCC patients and which have defects in maturation into dendritic cells able to stimulate T-cell reactivity [11,12]. Our prior in vitro studies had shown that 1 α ,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ] induced maturation of immune suppressive CD34 + progenitor cells into immune stimulatory dendritic cells [13,14]. Expanding this to a pilot clinical trial with HNSCC patients showed that 1,25(OH) 2 D 3 diminishes intratumoral levels of tumor-induced immune inhibitory CD34 + cells.…”

Section: Introductionmentioning

confidence: 99%

“…Our prior in vitro studies had shown that 1 α ,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ] induces maturation of immune suppressive CD34 + progenitor cells into immune stimulatory dendritic cells [13,14]. Expanding this to a pilot clinical trial with HNSCC patients showed that 1,25(OH) 2 D 3 diminishes intratumoral levels of tumor-induced immune inhibitory CD34 + cells.…”

Section: Introductionmentioning

confidence: 99%

Use of α,25-Dihydroxyvitamin D3 treatment to stimulate immune infiltration into head and neck squamous cell carcinoma

et al. 2010

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Prior studies have shown that treatment of head and neck squamous cell carcinoma (HNSCC) patients with 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] reduced intratumoral levels of immune inhibitory CD34+ progenitor cells while increasing levels of mature progeny dendritic cells. This finding was extended to a pilot study to determine whether 1,25(OH)2D3 treatment concurrently increases levels of intratumoral CD4+ and CD8+ T cells, increases intratumoral levels of immune cells expressing the early activation marker CD69, and prolongs time to HNSCC recurrence. The clinical trial comprised 16 patients with newly diagnosed HNSCC being untreated and 16 patients being treated with 1,25(OH)2D3 during the 3-week interval between cancer diagnosis and surgical treatment. Immunologic effects of treatment were monitored by immunohistochemical analyses of surgically removed HNSCC. Clinical effectiveness of 1,25(OH)2D3 treatment in this study was measured by the time to HNSCC recurrence. HNSCC tissues of patients who received treatment with 1,25(OH)2D3 contained increased levels of CD4+ cells and, more significantly, CD8+ T cells. Also prominent was an increase in cells expressing the lymphoid activation marker CD69. Results of this pilot study suggest that patients treated with 1,25(OH)2D3 had a lengthier time to tumor recurrence compared with patients who were not treated before surgery.

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Skewed differentiation of bone marrow CD34+ cells of tumor bearers from dendritic toward monocytic cells, and the redirection of differentiation toward dendritic cells by 1α,25-dihydroxyvitamin D3

Cited by 22 publications

References 30 publications

The tumour-induced systemic environment as a critical regulator of cancer progression and metastasis

The tumour-induced systemic environment as a critical regulator of cancer progression and metastasis

Improving cancer immunotherapy by targeting the STATe of MDSCs

Use of α,25-Dihydroxyvitamin D3 treatment to stimulate immune infiltration into head and neck squamous cell carcinoma

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